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anti-Mouse (Murine) Transferrin Receptor 2 Anticorps:
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Tfr2 is a key regulator of brain iron homeostasis and propose a role for Tfr2 alpha in the regulation of anxiety circuits.
these data confirm the role of Tfr2a in modulation of erythropoiesis and of Tfr2b in favoring iron availability for erythropoiesis
erythroid Tfr2 is essential for an appropriate erythropoietic response in iron-deficient anemia
These studies further elucidate the role of TFR2 in the regulation of iron homeostasis and its role in regulation of ferroportin and thus macrophage iron homeostasis
Tfr2 is a novel target gene for HNF4alpha, and hepatic HNF4alpha plays a critical role in iron homeostasis.
There is an essential role for TFR2 in erythropoiesis that may provide new targets for the treatment of anaemia.
We suggest that Tfr2 is a component of a novel iron-sensing mechanism that adjusts erythrocyte production according to iron availability, likely by modulating the erythroblast Epo sensitivity.
We propose that TFR2 is a limiting factor for erythropoiesis, particularly in conditions of iron restriction.
These results support in vivo studies which suggest that Hfe and Tfr2 can independently regulate hepcidin.
we used microarray and real-time reverse transcription polymerase chain reaction to assess brain transcriptome profiles of transferrin receptor 2 mutant mice a model of a rare type of hereditary hemochromatosis
Double mutant mice lacking functional Hfe or Tfr2 and Tmprss6 exhibited a severe iron deficiency microcytic anemia phenotype mimicking the phenotype of single mutant mice lacking functional Tmprss6 demonstrating that Hfe and Tfr2 are not substrates for Tmprss6.
Disruption of both Hfe and Tfr2 caused more severe hepatic iron overload with more advanced lipid peroxidation, inflammation, and portal fibrosis than was observed with the disruption of either gene alone.
Tfr2 is not essential for Hfe-mediated induction of hepcidin expression, supporting the possibility that TFR2 may regulate iron metabolism in an HFE-independent manner.
transferrin receptor 2 and HFE are involved in holotransferrin-dependent signaling for the regulation of furin which involved Erk phosphorylation. Furin in turn may control hepcidin expression.
that TfR2 exhibits a non hepatic function as a component of the EpoR complex and is required for efficient erythropoiesis.
A small reduction in hepatic transferrin-bound iron uptake in Tfr2 mutant mice suggests that Tfr2 plays a minor role in liver iron transport and its primary role is to regulate iron metabolism.
Our results strengthen the function of hepatic alpha-Tfr2 in hepcidin activation, suggest a role for extrahepatic Tfr2 and indicate that beta-Tfr2 may specifically control spleen iron efflux.
Hfe is limiting in formation of the Hfe/Tfr2 complex that regulates hepcidin expression
Hepcidin mRNA expression in vitro is highly sensitive to the presence of serum factors and PI3 kinase inhibition and parallels TfR2 expression
targeted mutagenesis of the murine transferrin receptor 2 gene produces hemochromatosis
In agreement with previous studies with truncated forms of these receptors, holo-Tf binds to the TfR1 homologue significantly stronger than to TfR2.
Authors retrospectively investigated whether TFR2 isoforms and EPOR are differentially expressed in MDS patients and whether the expression is associated with patients' clinical outcomes.
unreported iron metabolism-related genes in non-classic hereditary hemochromatosis patients that were predicted to be potentially pathogenic were three novel mutations in TFR2 [two missense (p.Leu750Pro and p.Ala777Val) and one intronic splicing mutation (c.967-1G>C)], one missense mutation in HFE (p.Tyr230Cys), and one mutation in the 5'-UTR of HAMP gene (c.-25G>A)
TFR2 expression altered within 4h of HAMP treatment, while HFE expression altered later at 24h and 48h, suggesting that TFR2 may function prior to HFE in HAMP regulation.
Of the non-HFE forms of iron overload, TFR2-, HFE2-, and HAMP-related forms are predicted to be rare, with pathogenic allele frequencies in the range of 0.00007 to 0.0005. Significantly, SLC40A1 variants that have been previously associated with autosomal-dominant ferroportin disease were identified in several populations (pathogenic allele frequency 0.0004), being most prevalent among Africans
Transferrin facilitates the formation of DNA double-strand breaks (DNA-DSBs) via transferrin receptor TfR1 but not TfR2.
In line with a status of iron deficiency, gene expression studies suggested decreased expression of transferrin and transferrin receptor 2 in non-alcoholic steatohepatitis livers
Our results indicate that membrane transferrin receptor-2, a sensor of circulating iron, is released from the cell membrane in iron deficiency.
results suggest that down-regulation of CD81 by GRAIL targets TfR2 for degradation
Polymorphisms of the TRF2 gene may be associated with age-related macular degeneration occurrence, either directly or by modulation of risk factors.
The variants of rs2075674 and rs7385804 in TFR2 gene were not associated with coronary heart disease risk in a Chinese Han population.
Present findings support the hypothesis of a main role of the TFR2 gene in HH pathogenesis in those regions, such as Central-Southern Italy, where the p.C282Y frequency is low.
Authors investigated the expression of TfR1 and TfR2 in human HCC tissues by immunohistochemistry, the first report demonstrating TfR2 expression immunohistochemically in human HCC.
N-linked glycosylation is dispensable for the cell surface expression and holo-Tf binding, but it is required for efficient intersubunit disulfide bond formation and holo-Tf-induced stabilization of TfR2.
Studies indicate that several genes have been linked to iron homeostasis, including transferrin (TF), iron regulatory protein 1 (ACO1) and transferrin receptor 2 (TFR2).
The hemochromatosis proteins HFE, TfR2, and HJV form a membrane-associated protein complex for hepcidin regulation.
Mutations in the TFR2 gene is associated with hemochromatosis.
TF, TFR2 and TMPRSS6 polymorphisms are significantly associated with decreased iron status, but only variants in TMPRSS6 are genetic risk factors for iron deficiency and iron-deficiency anemia.
Data sugggest that TfR-lytic peptide might provide a potent and selective anticancer therapy for patients.
TfR2 mRNA expression in hyperplastic anemia patients increases and closely correlates with hyperplasia status of bone marrow and anemia level in peripheral blood.
One novel SNPs was identified in TFR2 which tended to be associated (P < 0.013) with skeletal muscle iron content.
TfR2 is coexpressed with transferrin-a in the liver of the zebrafish embryo. Knockdown of TfR2 fails to produce anemia or a morphologic defect.
This gene encodes a single-pass type II membrane protein, which is a member of the transferrin receptor-like family. This protein mediates cellular uptake of transferrin-bound iron, and may be involved in iron metabolism, hepatocyte function and erythrocyte differentiation. Mutations in this gene have been associated with hereditary hemochromatosis type III. Alternatively spliced transcript variants encoding different isoforms have been described for this gene.
transferrin receptor 2
, transferrin receptor protein 2-like
, transferrin receptor protein 2